The mechanisms by which ischemia and hemorrhagic necrosis of the spinal cord are produced after a compressive lesion. Destruction of long tract axons, including their myelin coat, is the fundamental cause of paraplegia following cord injury. We propose to investigate the nature and topology of the "locomotor control system" in the monkey, defined as that set of neural elements whose integrity may be critical for "walking". Spasticity and other symptoms of abnormally exaggerated neuronal activity are often a delayed consequence of spinal cord injury in man. Often they are even more disabling than the losses of motor power and sensation. The molecular mechanisms of "supersensitivity of denervation" will also be studied related to the role of cyclic nucleotide systems. Interruption of a possible spinal ascending inhibitory system by hemisection of the spinal cord at the mid-thoracic level restores the tactile placing which is lost after bulbar pyramid section in cats.